Dizzy Vertigo

Med Clin N Am 90 (2006) 291–304

Diagnosis and Management of Dizzinessand Vertigo

Nancy Chawla, MDa,*, Jonathan S. Olshaker, MDa,b

aDepartment of Emergency Medicine, Boston University Medical Center, Boston, MA, USAbBoston University School of Medicine, Boston, MS, USA

Dizziness is the third most common complaint among all outpatients andthe single most common complaint among patients older than 75 years [1].These patients present to psychiatry clinics, emergency departments, andoutpatient offices. In all of these settings, the amount of time that the clini-cian has to spend with the patient is limited. Chronic cases average five phy-sician visits without resolution (Charles Yanofsky, MD, unpublished data,2004). For the patient, the ongoing dizziness and imbalance can lead toloss of function, falls, and injuries.

The evaluation of the dizzy patient can certainly be overwhelming for anyclinician. Few other complaints have such a broad differential. Dizziness asa chief complaint encompasses weakness, presyncope, neurologic impair-ment, vertigo, visual disturbance, and psychologic illness. Often difficultand time-consuming to handle, the dizzy patient is commonly referred tomedical specialists. Although otolaryngology, neurology, and cardiologyall play an important role in the evaluation of the patient, a good historyand focal physical examination in the primary care setting can usually revealthe diagnosis.

In addition to diagnosing the patient, the goal of the primary clinicianshould be to recognize which patients need inpatient management or emer-gent intervention. This goal becomes particularly important when evaluat-ing older patients. Several acute pathologic conditions can present withdizziness as the initial complaint. This article outlines the diagnostic ap-proach to the dizzy patient, with emphasis on the differentiation of clinicalemergencies.

* Corresponding author. Department of Emergency Medicine, Boston University Medical

Center, One Boston Medical Center Place, Dowling One South, Boston, MA 02118.

E-mail address: [email protected] (N. Chawla).

0025-7125/06/$ - see front matter � 2006 Elsevier Inc. All rights reserved.

doi:10.1016/j.mcna.2005.11.003 medical.theclinics.com

mailto:[email protected]

292 CHAWLA & OLSHAKER

Diagnostic approach

History

Obtaining a good history is the most critical step in the assessment of thedizzy patient. Because the term dizzy is used by patients to describe a varietyof experiences, it is important to clarify the patient’s actual complaint. Thesensation of movement or spinning is classic for true vertigo. These patientsmay complain of objects moving around them (objective vertigo) or thatthey are spinning relative to their surroundings (subjective vertigo). Otherpatients may describe light-headedness or weakness. These symptomsshould guide the clinician to investigate more systemic diseases consistentwith presyncope.

Often, a good history can elicit whether a patient has true vertigo andwhether the cause is central or peripheral. Vertigo, which is peripheral in or-igin, often presents as severe, intense attacks that last several seconds to mi-nutes. Occasionally, more severe episodes last up to several hours and areaccompanied by nausea, vomiting, and disequilibrium. Vertigo triggeredby a change in position is also suggestive of a peripheral disorder. A centraletiology is more concerning in patients who describe mild symptoms that aregradual in onset and last several weeks to months (Table 1).

It is also important for the physician to inquire about associated symp-toms. Diseases of the middle and inner ear can cause hearing loss, aural full-ness, and tinnitus along with vertigo. The physician should attempt tolocalize the auditory symptoms to one side. The symptomatic ear is oftenthe one with vestibular damage. Associated neurologic symptoms aremore consistent with central vertigo. Headaches may suggest dizziness asso-ciated with migraines. Other symptoms suggestive of a central disorder in-clude visual changes, seizures, ataxia, or other gait disturbances. Thepresence of these symptoms should provoke further investigation andimaging.

A thorough medication history should also be reviewed. Several drugsare directly ototoxic and should be discontinued in any patient complainingof vertigo. These drugs include certain aminoglycosides, furosemide,

Table 1

Characteristics of peripheral and central vertigo

Characteristic Peripheral Central

Severity Severe Mild

Onset Sudden Gradual

Duration Seconds to minutes Weeks to months

Positional Yes No

Fatigable Yes No

Associated symptoms Auditory Neurologic and visual

Associated nystagmus Horizontal Vertical

293DIZZINESS & VERTIGO: DIAGNOSIS & MANAGEMENT

ethacrynic acid, acetylsalicyclic acid, amiodarone, quinine, and cisplatinum.Psychotropic medications are also notorious for causing light-headednessand disequilibrium (Box 1), of which the most commonly encountered areanti-Alzheimer’s medications, anticonvulsants, antidepressants, and anxio-lytics. In addition, chronic use of vestibular suppressants such as meclizineand scopolamine may result in sensitization. Patients can have severe with-drawal symptoms when these medications are discontinued. A variety ofmedications can induce toxic labyrinthitis. In these cases, the offending med-ication should be immediately discontinued.

A complete social history is also important in patients complaining ofdizziness. Alcohol, nicotine, and caffeine can all exacerbate vertiginoussymptoms. Current or previous use of illicit drugs should be documented.Sexual history should also be noted. Certain sexually transmitted diseasessuch as syphilis have otologic symptoms. In addition, any history of trau-matic head injury or cervical trauma should be investigated. Finally, it is im-portant to remember that depression and anxiety can also manifest asdizziness.

Physical examination

After a good history has been obtained, the next important step is a thor-ough physical examination. Particular emphasis should be placed on the oc-ular examination. It is important to test pupillary reactivity and extraocularmovements. Subtle ocular abnormalities can sometimes be the only clue tocerebellar disease. A fundoscopic examination should always be performed.

Box 1. Psychotropic medications that may cause dizziness

Anti-Alzheimer’s (memantine, rivastigmine, tacrine)Antipsychotics

� Typicals (chlorpromazine, prochlorperazine, fluphenazine,perphenazine, thioridazine, trifluoperazine)

� Atypicals (all except olanzapine)Antidepressants

� Selective serotonin reuptake inhibitors (all)� Tricyclics (amitriptyline, nortriptyline, trazodone,

imipramine)� Monoamine oxidase inhibitors (selegiline, phenelzine)� Others (nefazodone, venlafaxine, mirtazapine, bupropion)

Anxiolytics (alprazolam, clonazepam, diazepam, lorazepam,oxazepam, chlordiazepoxide)

Mood stabilizers (gabapentin, carbamazepine, oxcarbazepine,lamotrigine)

Anticonvulsants (phenytoin)


Papilledema usually presents bilaterally and is indicative of elevated intra-cranial pressure. In these patients, vision is usually is well preserved and vi-sual acuity testing does not offer significant additional information.

In patients who have unilateral vestibular disorders, horizontal beatingnystagmus may be observed away from the side of the lesion. The abnormaljerk nystagmus that is classical for inner ear disease consists of slow andquick components. Patients exhibiting coarse vertical nystagmus may havea central lesion which is thought to be related to asymmetric vestibular inputfrom both sides. Patients who have peripheral vestibular disease should beable to suppress the nystagmus by focusing their vision on a stationary tar-get. The inability to suppress the nystagmus is suggestive of a central abnor-mality. It is often helpful to ask the patient’s family whether they noted anyunusual eye movements during the acute vertiginous episode which is partic-ularly important with pediatric patients [2].

If nystagmus is not present at rest, then positional testing should be per-formed. The patient’s eye movement should be noted while lying supine withthe head extended and turned to one side. The test should be repeated withthe head turned to the other side. Positional nystagmus is strongly sugges-tive of vestibular disease. This maneuver often reproduces vertiginous symp-toms in patients who have a peripheral disorder. Because of the risk ofdislodging atheromatous plaques in the vertebrobasilar vessels with suddenturning movements, this maneuver should be avoided in elderly patients.

When examining the ear, the clinician should use an otoscope to look forimpacted cerumen or any foreign object in the ear canal. Often, removal ofthe foreign body relieves the symptoms of vertigo. It is also important torecognize signs of middle ear disease such as fluid behind the eardrum, per-foration, or extensive scarring. The patient should be tested for any subtlehearing loss. If the hearing is abnormal, the Rinne and the Weber’s tun-ing-fork tests can help determine whether the hearing loss is conductive orsensorineural.

The heart and carotid arteries should be auscultated because occasionally,a positive finding points to vascular causes of dizziness. Examinations signif-icant for a carotid bruit, heart murmur, or irregular rhythm should impressupon the physician the need for a cardiovascular work-up. This work-up isparticularly important in older patients or those who are at high risk for ce-rebrovascular disease.

A thorough neurologic examination is important in patients complainingof dizziness. A complete cranial nerve evaluation may help localize lesions ofthe midbrain, pons, and medulla. The patient’s cerebellar function can beassessed with finger-to-nose pointing and rapidly alternating movements.Romberg’s test is also useful in assessing the dizzy patient. The patient isasked to stand with feet together and arms folded. The inability to maintainposture in this position is suggestive of abnormal proprioception.

Any gait abnormality should arouse suspicion of a central lesion. Themain features of an ataxic gait consistent with cerebellar disease are


a wide base, unsteadiness, irregularity of steps, tremor of the trunk, andlurching from side to side. This unsteadiness is most prominent on arisingquickly from sitting, turning sharply, and stopping suddenly while walking.

Laboratory tests

Most routine testing is not helpful in the evaluation of the patient whohas vertiginous symptoms; however, in the absence of clinical findings orin the evaluation of the patient who has near syncope, a complete bloodcount and chemistry panel can be helpful. Some clinicians also recommendthyroid function tests, fasting glucose, and rheumatoid factor [3].

Electrocardiography

Because myocardial ischemia can present atypically in many patients, it isimportant to obtain an ECG on those patients who are older or have signif-icant cardiac risk factors. In addition, any patient who requires an emergencyroom evaluation after being seen in the outpatient office should have an ECGreviewed before transfer.

Electronystagmography

Electronystagmography is an examination that records eye movements inresponse to vestibular, visual, cervical, caloric, rotational, and positionalstimulation [4]. Electrodes are placed at the outer and inner canthi for hor-izontal recordings and above and below the eye for vertical recordings. Elec-tronystagmography testing is helpful in assessing vestibular dysfunction butis limited in diagnosing nonvestibular disorders [5].

Radiologic imaging

When cerebellar hemorrhage, cerebellar infarction, or other central le-sions are suspected, an emergent CT or MRI of the brain is indicated. Thesepatients should be immediately transferred to an emergency department thathas neuroimaging capabilities.

In patients at particularly high risk for cerebrovascular disease, magneticresonance angiography can be used to visualize the intracranial vasculature.Although a less sensitive study than cerebral angiography because of its lim-ited visualization of small vessels, magnetic resonance angiography remainsmore readily used by neurologists to evaluate high-risk patients.

MRI with gadolinium enhancement is particularly useful in detectingsmaller intracanalicular tumors such as acoustic neuromas. It is also recom-mended for identifying sclerotic and demyelinating white matter lesions char-acteristic of multiple sclerosis. Although not indicated in younger patientswho have a clear peripheral cause, radiologic imaging should be consideredin all patients who have new-onset vertigo or neurologic findings [6,7].


Peripheral vertigo

Peripheral causes of vertigo arise from abnormalities in the vestibular endorgans (semicircular canals and utricle), the vestibular nerve, and the vestib-ular nuclei. Most of these causes are benign and readily treatable.

Benign paroxysmal positional vertigo

The most common cause of peripheral vertigo is benign paroxysmal po-sitional vertigo (BPPV). As the name implies, this condition is paroxysmal(sudden onset) and positional. Most patients report attacks provoked byturning their head. BPPV is characterized by its fatigability. The patient de-velops a tolerance to head movements, leading to a reduction in symptoms.

The condition occurs when debris (otoconia) from the utricle circulateswithin the endolymphatic system, causing positional irritation of the cupulaand stimulating vertigo and nystagmus. Occasionally, the debris attaches tothe cupula (cupulolithiasis) and symptoms persist for weeks.

The treatment of acute attacks of BPPV centers around symptomatic re-lief. Benzodiazepines, intravenously and orally, effectively relieve vertigi-nous symptoms because of their sedative effect. Anticholinergics andantihistamines have also been shown to be helpful in alleviating symptomsby mediating the amount of acetylcholine involved in vestibular reactions. Ashort course of meclizine or diphenhydramine may resolve the vertiginoussymptoms. Antiemetics such as promethazine may improve the nausea asso-ciated with vertigo.

Canolith repositioning procedures treat BPPV by directing the otoconiaback to the utricle where it is absorbed. The Epley and Semont maneuvershave been shown to be 85% to 95% effective in treating patients who haveBPPV [8–10]; however, in more than half of patients, a recurrence of symp-toms occurs [11]. In these cases, patient education and reassurance areimportant.

Otitis media

Patients who have otitis media often complain of vertigo. Because of theproximity of the vestibular end organs to the middle ear, the infectious pro-cess may extend to these structures. These patients are at risk for hearing lossand often end up with permanent labyrinthe deficits if left untreated. Exten-sion of the infection into the mastoid can also occur, and these patients maydevelop an epidural abscess. With the early use of antibiotics and the treat-ment of the underlying otitis, these complications can usually be avoided.

Labyrinthitis

Labyrinthitis is a peripheral disorder characterized by inflammation of thecanals of the inner ear. The cause of labyrinthitis is unknown, but because it


commonly occurs following otitis media or an upper respiratory infection, itis thought to be a consequence of viral or bacterial infection [12]. It may alsofollow allergy, cholesteatoma, or the ingestion of certain drugs that are toxicto the inner ear. Patients who have acute labyrinthitis usually present withsevere vertigo, hearing loss, nausea, vomiting, and fever.

Bacterial infections may directly invade the perilymphatic space, causinga suppurative labyrinthitis. These infections usually extend from the middleear through a ruptured membrane or perilymph fistula. In patients who havemeningitis, the infected cerebrospinal fluid enters the labyrinth through thecochlear aqueduct or internal auditory canal.

Patients who have bacterial labyrinthitis appear ill and require hospitaladmission and intravenous antibiotics. Occasionally, these patients alsoneed surgical drainage and debridement. Bacterial labyrinthitis is one ofthe few causes of peripheral vertigo that requires early detection and transferto the emergency department.

Vestibular neuritis

Vestibular neuritis usually results as a complication of an upper respira-tory infection. The prevalence of vestibular neuritis peaks at age 40 to 50years [13]. The virus affects the vestibular nuclei and causes sudden and se-vere vertigo, nausea, and vomiting. Auditory symptoms are usually absent.The diagnosis can be made on clinical presentation alone. Treatment withprednisone in the first 10 days of the attack may shorten the course of theillness. The acute attack is debilitating and patients often require bedrest.

Ramsay Hunt syndrome is caused by varicella zoster and is a variant ofvestibular neuritis, with involvement of cranial nerves VII and VIII. Itcauses facial paresis, tinnitus, hearing loss, and a vestibular defect [14]. Pa-tients who have Ramsay Hunt syndrome respond well to early initiation ofprednisone and acyclovir.

Cholesteatoma

Cholesteatoma is a benign skin growth that occurs in the middle ear be-hind the ear drum. It is usually due to repeated infection, which causes aningrowth of the skin of the eardrum. Over time, the cholesteatoma can in-crease in size and destroy the surrounding delicate bones of the middleear. When this benign tumor erodes into the labyrinthe, it causes hearingloss and vertigo. The vertigo tends to be severe in these patients but typicallydoes not last beyond a few seconds. Surgical removal of the cholesteastomais indicated in symptomatic patients.

Trauma

The incidence of dizziness and dysequilibrium following head or neck in-jury is between 40% and 60%, even following mild or moderate head


injuries not requiring acute hospitalization [15]. Any evidence of significanttraumatic injury should incite a complete trauma evaluation [16]. Blunt headinjury can concuss the membranous labyrinth with preservation of the oticcapsule. Patients may complain of mild vertigo, disequilibrium, and nausea[17]. Symptoms tend to resolve spontaneously over several days to weeks.

Explosive blasts can also result in symptoms of vertigo. Pressure wavesclassically injure the ear by rupturing the tympanic membrane and disrupt-ing the ossicular chain. The cochlea and hair cells can shear off the basilarmembrane, causing significant inner ear damage.

Barotrauma to the inner ear is rare. It results from acute changes in at-mospheric pressure. Deep-sea divers and pilots are particularly at risk forthis type of injury. A perilymphatic fistula occurs when there is rupture ofthe oval or round windows that separate the perilymphatic space from themiddle ear. Patients who have perilymphatic fistulas from barotrauma usu-ally complain of a sudden onset of vertigo or dizziness. Patients are put onbedrest for 1 to 2 weeks and instructed to avoid any activities that wouldproduce Valsalva-type maneuvers. Most patients heal spontaneously, butsurgical repair is recommended in severe cases.

Endolymphatic hydrops

The most common form of endolymphatic hydrops is Meniere’s disease.Patients may present with the classic triad of tinnitus, fluctuant sensorineu-ral hearing loss, and vertigo. The vertigo attacks may last several minutes toan hour. It is not typical for these attacks to persist longer than severalhours. As the disease progresses, attacks occur more frequently and aremore severe. Although the disease starts unilaterally, almost half of patientsdevelop bilateral auditory symptoms.

The predominant pathology of Meniere’s disease is dilation of the endo-lymphatic system caused by excess production of endolymph or decreasedreabsorption. Because salt in the diet is thought to increase the endolym-phatic volume, the cornerstone of medical treatment involves salt restrictionand diuretics. Greater than 90% of patients respond well to medical man-agement [18]. For patients in whom medical therapy is not effective, surgicaloptions include endolymphatic sac decompression or shunting, vestibularnerve resection, or labyrinthectomy. Chemical ablation of the vestibular ap-paratus has also gained wide acceptance as a treatment modality. In thesecases, gentamycin is injected transtympanically. Although a less aggressiveapproach than surgery, chemical ablation has a greater risk of hearing loss.

Acoustic neuroma

An acoustic neuroma is a tumor composed of the Schwann cells of thevestibular nerve. Although vertigo is the most common presenting symp-tom, it is often associated with unilateral hearing loss or tinnitus [19]. In


patients who have suspected acoustic neuroma, a gadolinium-enhancedMRI should be ordered. The MRI detects intracanalicular abnormalitieswith 100% sensitivity and is the ‘‘gold standard’’ for detecting this tumor.Because there is a potential for the tumor to expand intracranially, the pa-tient should be reimaged regularly [20,21]. Treatment options include radio-therapy or surgical removal.

Central vertigo

Central vertigo manifests as marked vertigo, nausea, and vertical nystag-mus. Neurologic symptoms such as headache or gait ataxia may also bepresent. In severe cases, patients may have depressed levels of consciousness.The cerebellum is often involved, and etiologies include multiple sclerosis,tumor, hemorrhage, and ischemia. Vascular injuries and infarcts of the cen-tral neurologic system can cause permanent debilitating disease. Becausecentral processes have more serious consequences, aggressive work-up andtreatment are recommended.

Even in patients who have mild symptoms, it is important to maintaina high level of clinical suspicion when advanced age, atrial fibrillation, hy-pertension, or previous cerebrovascular disease is present. Often, vertigo isthe only presenting symptom in patients who have impending infarction.When a central etiology is suspected, the patient should be transferred im-mediately by ambulance to an emergency department for neurologic imag-ing. Evaluation by neurology and neurosurgery may be needed.

Cerebellar hemorrhage

In patients who have acute neurologic deficit, it is often difficult to distin-guish intracranial hemorrhage from ischemic infarct. It is imperative not toadminister anticoagulant medicine, including aspirin, until intracranial hem-orrhage has been ruled out by imaging. Because the posterior fossa is a rel-atively small and nonexpandable space, hemorrhage can lead to rapidcompression and compromise of vital medullary functions, obstructive hy-drocephalus, or herniation of the medullary tonsils. Endotracheal intuba-tion may be needed to protect the airway, control breathing, and allowtherapeutic hyperventilation. Because neurosurgical consultation may beneeded for surgical decompression by way of suboccipital craniectomy orventriculostomy, all patients who have a presentation of central diseaseshould be transferred only to centers that have neurosurgical capabilities.

Brainstem ischemia

Vertigo may occur from infarcts in the posterior fossa that contain ves-tibular pathways. The cerebellar circulation is complex, and it is often diffi-cult to localize the area of ischemia without magnetic resonanceangiography.


The anterior inferior cerebellar artery divides into several branches thatperfuse the lateral cerebellum, the pons, and the labyrinth. Several typesof anterior inferior cerebellar artery syndromes result in acute vertigo. In-farct of the anterior vestibular artery can present with peripheral symptomsonly. Infarct of the common cochlear artery causes peripheral symptomsand hearing loss and tinnitus. Patients who have infarcts of the pontinebranch can present with central signs such as dysarthria, facial palsy, sensoryloss, Horner syndrome, and dysmetria [22].

The posterior inferior cerebellar artery perfuses part of the cerebellumand the dorsolateral medulla. Infarcts in the lateral medulla often damagethe vestibular nucleus and cause vertigo. This condition is known as Wallen-berg syndrome and characterized by crossed sensory signs, ipsilateral later-opulsion, ataxia, and Horner’s sign.

Vertebrobasilar insufficiency

Vertebrobasilar insufficiency occurs when there is narrowing of the ar-teries that supply the posterior brain (subclavian, vertebral, or basilar ar-teries). It is usually the result of hardening of the arteries (atherosclerosis)and occurs among patients older than 50 years. The narrowed arteries de-crease the blood flow and, therefore, the oxygen to the vestibular centerin the brain. Because the vestibular system is very sensitive to a lack of ox-ygen, difficulty with balance is often one of the first symptoms of vertebro-basilar insufficiency.

Transient ischemic attacks from vertebrobasilar ischemia provoke epi-sodes of dizziness that are abrupt and usually last only a few minutes.They are frequently associated with other symptoms, most commonly visualdisturbance, drop attacks, unsteadiness, or weakness. Changing or rapidlyprogressive symptoms should also raise suspicions of impending posteriorcirculation occlusion.

Vertebrobasilar insufficiency should be considered in any patient of ad-vanced age who has new-onset vertigo without an obvious cause [6]. Thesepatients should be evaluated by and admitted to the neurology service. Mag-netic resonance arteriography can be performed to assess posterior circula-tion vessels and transcranial Doppler may detect decreased flow in thebasilar artery. Treatment includes reduction of risk factors for cerebrovascu-lar disease and antiplatelet therapy. Warfarin is used when there is significantvertebral or basilar artery stenosis [23]. Fig. 1 summarizes the managementand disposition for patients who have central or peripheral vertigo.

Dizziness

In patients who complain of dizziness without clear vertiginous symp-toms, the differential remains broad. Many patients complain of disequilib-rium and imbalance, whereas others note light-headedness and other


presyncope symptoms. Often, dizziness can be a multisensory disorder dueto any combination of peripheral neuropathy, visual impairment, and mus-culoskeletal disease.

Proprioceptive abnormalities

Many diseases directly affect the proprioceptive sensory fibers. Chronicalcoholism is among the diseases manifesting with symptoms of dizzinessand imbalance. These patients may have deterioration of the vestibulospinalpathways. These symptoms are usually not reversible and the patient mustbe counseled on safety and fall risk. Chronic alcoholism can also lead to

Benign paroxysmal positional vertigoSymptomatic reliefRepositioning maneuver

Acute suppurative labyrinthitisIV AntibioticsOtolaryngology consultHospital admission

PeripheralVertigo

Vestibular neuritisPrednisone

TraumaTrauma evaluationSymptomatic relief

VertigoHistoryPhysicalFinger stick glucoseElectrocardiogram

Endolymphatic hydropsSalt restrictionDiuretics

Acoustic neuromaMagnetic resonance imagingOtolaryngology consult

Cerebellar hemmorhageEmergent neuroradiological imagingEmergent neurosurgery consult

Brainstem ischemiaNeuroradiological imagingNeurology consultHospital admission

CentralVertigo

Vertebrobasilar insufficiencyNeuroradiological imagingNeurology consultHospital admission

Fig. 1. Management of vertigo.


compromised vitamin absorption from the gastrointestinal tract, leading toperipheral neurologic changes.

Syphilis is another rare but important cause of dizziness. In tertiary syph-ilis (tabes dorsalis), there is a deterioration of the posterior columns. Thesepatients have compromised proprioception and often complain of difficultywalking in the dark.

Cerebral anoxia

A number of conditions can lead to poor blood flow to the central ner-vous system. These patients do not classically complain of light-headednesswhile sitting or lying down. Their symptoms can usually be reproduced withstanding. Anemia may produce cerebral anoxia and can result from anynumber of causes. Iron deficiency, malignancy, vitamin deficiency, andchronic blood loss are some examples. Patients who have significant arterio-sclerosis may also complain of positional symptoms. In these patients, otherneurologic symptoms including weakness and syncope may be present.

Orthostatic hypotension is often seen in patients who complain of dizzi-ness when arising to a standing position. The symptoms are generally tran-sient and resolve spontaneously. In these cases, medication-inducedhypotension must be ruled out. Often, no underlying cause is found forthe autonomic response.

Metabolic disorders

Many patients who have thyroid dysfunction can present with dizzinessas an initial complaint. Many patients also have dizziness associated withpregnancy or menstruation. It has been well documented that acute changesin hormone levels commonly lead to symptoms of light-headedness. Hypo-glycemia can also cause dizziness. In patients who do not have an obviousdiagnosis, a finger-stick blood glucose should be performed [24].

Migraines

The mechanism of dizziness or vertigo from migraines is unknown. Mi-graine is a vascular disease characterized by periodic, unilateral headaches.These headaches are often preceded for a variable time by associated neuro-logic symptoms called the aura. In individuals who have migraine, dizzinessand vertigo can occur as part of the aura or separately. Spells usually lastapproximately an hour but can last several hours or days in patients whohave severe symptoms. Most patients who have migraines have a long his-tory of recurring symptoms.

The management of migraine is divided into two categories: symptomaticand preventive treatments. Acute attacks can be treated with various nonop-ioid analgesics. Preventive treatment is most frequently accomplished withamitryptiline, b-blockers, calcium channel blockers, and acetazolamide.


Acetazolamide has been particularly effective in treating patients who havevestibular symptoms associated with migraine.

Presyncope

Presyncopal patients complain of feeling faint and light-headed withoutlosing consciousness. Sometimes nausea, dizziness, diaphoresis, and a senseof warmth accompany a feeling of faintness. Patients who have a history ofunexplained fainting or recurring presyncope often need an inpatient evalu-ation to investigate cardiac causes of their symptoms. The work-up andtreatment of these patients is discussed more thoroughly in articles onsyncope.

Psychogenic

Psychogenic dizziness often occurs in patients who have chronic anxiety.The complaints are often vague, numerous, and out of proportion to thephysical findings. In other patients, panic attacks manifest as sudden intensefear or discomfort and reach a crescendo within 10 minutes. They are fre-quently associated with brief episodes of dizziness, nausea, shortness ofbreath, chest tightness, paresthesias, and diaphoresis. Physical examinationfindings in patients who have psychogenic disorders are often dramatic.They include excessive slowness or hesitation, exaggerated sway on stand-ing, and sudden buckling of the knees.

Selective serotonin reuptake inhibitors are the mainstay of treatment forpanic disorders and chronic anxiety. Counseling and behavior modificationare also frequently helpful.

Summary

Dizziness and vertigo present in patients of all ages. Particularly in olderpatients, dizziness is associated with a variety of cardiovascular, neurosen-sory, and psychiatric conditions and with the use of multiple medications[25]. For the patient, the symptoms can be debilitating. In patients olderthan 60 years, 20% have experienced dizziness severe enough to affect theirdaily activities [26]. Appropriate diagnosis and treatment can significantlyimprove quality of life. Most causes of dizziness are benign, but early recog-nition of serious or life-threatening disease is important. Management ofthese patients includes referral for neuroimaging and further evaluation inan emergency department.

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Dizzy Vertigo